Inflammatory response of tracheobronchial epithelial cells to endotoxin

Neff, Simona B; Z’graggen, Birgit Roth; Neff, Thomas; Jamnicki-Abegg, Marina; Suter, Dominik; Schimmer, Ralph C.; Booy, Christa; Joch, Hana; Pasch, Thomas; Ward, Peter A.; Beck‐Schimmer, Beatrice

doi:10.1152/ajplung.00391.2004

Cited by 27 publications

(30 citation statements)

References 47 publications

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“…In addition, other pulmonary cells may contribute to the secretion of these cytokines in BALF. Several studies have suggested pulmonary epithelial cells as potential sources of TNF-a production, a theory that is supported by the fact that TNF-a protein has been localised to alveolar epithelial cells by immunohistochemical staining [30][31][32]. In contrast, according to the present data, the levels of IL-10 mRNA and protein in the BALF of sarcoidosis patients correlated well, indicating that BALF IL-10 was primarily produced by BALF cells in sarcoidosis.…”

Section: Discussionsupporting

confidence: 76%

Reduced Th1 response in the lungs of HLA-DRB1*0301 patients with pulmonary sarcoidosis

Idali

Wikén²,

Wahlström³

et al. 2006

European Respiratory Journal

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To investigate why human leukocyte-associated antigen-DRB1*0301 (HLA-DRB1*0301) positive Scandinavian patients have a better prognosis than HLA-DRB1*0301 negative patients, the present authors examined patterns of cytokine expression in bronchoalveolar lavage (BAL) cells and BAL fluid (BALF) from patients with pulmonary sarcoidosis and controls.Using real-time PCR, the mRNA expression of selected cytokines in BAL cells from newly diagnosed, untreated nonsmoking patients (n525) and controls (n511) was quantified. Cytokine protein levels in BALF from patients (n534) and controls (n511) were assessed using cytometric bead array. The patients were evaluated and stratified into two subgroups: HLA-DRB1*0301 positive (all with an acute onset) and HLA-DRB1*0301 negative (all with an insidious onset).When comparing patients and controls, BAL cells of the patients expressed significantly higher levels of interferon (IFN)-c and interleukin (IL)-10 mRNA. There were significantly decreased IFN-c and tumour necrosis factor (TNF)-a mRNA levels, and a tendency toward higher levels of transforming growth factor-b1 mRNA in HLA-DRB1*0301 positive compared with HLA-DRB1*0301 negative patients. Protein levels of IL-1b, IL-2, IL-6, IL-12p70 and TNF-a in BALF were significantly higher in patients. HLA-DRB1*0301 positive patients exhibited tendencies to lower levels of most cytokines in BALF.In conclusion, the present data show a reduced expression of T-helper cell type-1 cytokines in human leukocyte-associated antigen-DRB1*0301 positive patients, which may relate to their good prognosis.

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Section: Discussionsupporting

confidence: 76%

Reduced Th1 response in the lungs of HLA-DRB1*0301 patients with pulmonary sarcoidosis

Idali

Wikén²,

Wahlström³

et al. 2006

European Respiratory Journal

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“…This statement can also be applied to tracheobronchial epithelial cells. In a previous work from our group, we were able to demonstrate that the intrinsic apoptosis pathway is activated at 24 h of LPS stimulation [10]. Results of the current study show that the process of apoptosis is already initiated at earlier time-points upon stimulation with LPS.…”

Section: Discussionsupporting

confidence: 66%

“…At 4 h of injury, apoptosis rate decreased by 19% (range 35%) under hypoxia and by 32% (range 39%) with LPS, respectively (P < 0·05). In tracheobronchial epithelial cells, apoptosis increased upon 24 h of LPS stimulation, as shown previously with the help of a terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labelling (TUNEL) staining [10].…”

Section: Hypoxia-and Endotoxin-induced Apoptosis In Target Cellssupporting

confidence: 74%

Acute lung injury: apoptosis in effector and target cells of the upper and lower airway compartment

Z’graggen

Tornic

Müller‐Edenborn

et al. 2010

Clinical and Experimental Immunology

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SummaryApoptotic cell death has been considered an underlying mechanism in acute lung injury. To evaluate the evidence of this process, apoptosis rate was determined in effector cells (alveolar macrophages, neutrophils) and target cells (tracheobronchial and alveolar epithelial cells) of the respiratory compartment upon exposure to hypoxia and endotoxin stimulation in vitro. Cells were exposed to 5% oxygen or incubated with lipopolysaccharide (LPS) for 4, 8 and 24 h, and activity of caspase-3, -8 and -9 was determined. Caspase-3 of alveolar macrophages was increased at all three time-points upon LPS stimulation, while hypoxia did not affect apoptosis rate at early time-points. In neutrophils, apoptosis was decreased in an early phase of hypoxia at 4 h. However, enhanced expression of caspase-3 activity was seen at 8 and 24 h. In the presence of LPS a decreased apoptosis rate was observed at 8 h compared to controls, while it was increased at 24 h. Tracheobronchial as well as alveolar epithelial cells experienced an enhanced caspase-3 activity upon LPS stimulation with no change of apoptosis rate under hypoxia. While increased apoptosis rate is triggered through an intrinsic and extrinsic pathway in alveolar macrophages, intrinsic signalling is activated in tracheobronchial epithelial cells. The exact pathway pattern in neutrophils and alveolar epithelial cells could not be determined. These data clearly demonstrate that upon injury each cell type experiences its own apoptosis pattern. Further experiments need to be performed to determine the functional role of these apoptotic processes in acute lung injury.

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“…Apoptosis in cultured A549 cells [37] and tracheobronchial epithelial cells [38] treated with LPS has been reported only with very high doses of LPS (100 mg?mL -1 ), which are of questionable clinical significance. LPS-induced apoptosis in vivo probably is the result of more complex convergence of death signals, including the Fas/FasL pathway [8].…”

Section: Epo: Cytoprotective In Lung Epithelium R Macredmond Et Almentioning

confidence: 99%

Erythropoietin inhibits respiratory epithelial cell apoptosis in a model of acute lung injury

MacRedmond¹,

Singhera²,

Dorscheid³

2009

European Respiratory Journal

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Fas-mediated apoptosis of the alveolar epithelium is important in the pathogenesis of acute respiratory distress syndrome. Erythropoietin (EPO) has cytoprotective properties in other organ systems, and is relatively deficient in critical illness. This study investigates a potential role for EPO in reducing apoptosis in a model of acute lung injury.Apoptosis was induced in human alveolar epithelial (A549) cells or normal human bronchial epithelial (NHBE) cells by Fas activation with CH-11 Fas-crosslinking antibody or by co-culture with polymorphonuclear neutrophils in a transwell system. The effect of recombinant human (rh)EPO on apoptosis was measured by poly(ADP-ribose) polymerase cleavage and cell death detection assay. The specific EPO-EPO receptor (EPOR)-mediated effect was determined using an EPO-blocking antibody or EPOR small interfering RNA.Expression of EPOR was demonstrated in A549, NHBE and normal human alveolar epithelium. Fas-and neutrophil-mediated apoptosis of A549 and NHBE cells was inhibited by rhEPO by a specific EPO-EPOR-mediated mechanism. This anti-apoptotic effect was associated with induction of a pro-apoptotic Bcl-xL/Bax ratio.EPO has cytoprotective properties in respiratory epithelium in an in vitro model, which may indicate a potential therapeutic role in acute lung injury.

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Inflammatory response of tracheobronchial epithelial cells to endotoxin

Cited by 27 publications

References 47 publications

Reduced Th1 response in the lungs of HLA-DRB1*0301 patients with pulmonary sarcoidosis

Reduced Th1 response in the lungs of HLA-DRB1*0301 patients with pulmonary sarcoidosis

Acute lung injury: apoptosis in effector and target cells of the upper and lower airway compartment

Erythropoietin inhibits respiratory epithelial cell apoptosis in a model of acute lung injury

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